News Release

Study supports association between HPV infection and head and neck cancer

Peer-Reviewed Publication

Journal of the National Cancer Institute

A new study reports that head and neck squamous cell carcinomas (HNSCCs) that harbor transcriptionally active human papillomaviruses (HPV) have a different pattern of genetic changes than tumors without HPV. These patterns suggest that infection with HPV may play a role in the development of HNSCC, according to the study, which appears in the July 7 issue of the Journal of the National Cancer Institute.

HPV is known to cause most cases of cervical cancer. Some studies have suggested that the virus may also play a role in the development of HNSCCs, and HPV DNA has been detected in the tumors of 10% to 20% of HNSCC patients. In addition, active HPV DNA can be found in the tumors of HNSCC patients who do not drink or smoke--factors that have been associated with an increased risk of HNSCC. It is believed that HPV infection is an independent risk factor, but an interaction with exposure to tobacco smoke can not be excluded. The mechanism by which HPV might cause HNSCC is not known.

To find a possible mechanism of HPV carcinogenesis, Boudewijn J. M. Braakhuis, Ph.D., of the VU University Medical Center in Amsterdam, Netherlands, and colleagues looked at HPV DNA and RNA and genetic alterations in the tumors of 143 patients with HNSCC.

HNSCCs that had transcriptionally active HPV DNA (i.e., specific viral genes were expressed in the tumor cells) had a distinct genetic pattern in which there was little chromosomal loss. HNSCCs that lacked transcriptionally active HPV DNA had a genetic pattern in which whole or large parts of chromosomal arms were lost early in tumor development. The observed patterns support the idea that HNSCCs can be subdivided into two genetically distinct categories and that HPV infection is involved in the early development of some HNSCCs, according to the authors.

"Our results are consistent with the hypothesis that HNSCCs develop by two different etiologies: one driven by exposure to environmental carcinogens (i.e., tobacco and alcohol) without HPV involvement and the other involving infection with transcriptionally active [HPV]," the authors write.

In an editorial, Li Mao, M.D., and Waun Ki Hong, M.D., of the University of Texas M. D. Anderson Cancer Center in Houston, review the evidence linking HPV infection with HNSCCs. "Understanding how the [HPV] viral proteins interact with cellular proteins and/or DNA in host cells may allow us to design strategies to block malignant transformation," they write. "The promising results from a trial of an HPV vaccine to prevent cervical cancer raises hope that such a strategy can also be used to reduce the incidence of HNSCC."



  • Article: Jakomien ter Haar, VU University Medical Center, 31-20-444-3471,
  • Editorial: Laura Sussman, Media Office, M. D. Anderson Cancer Center, 713-792-0655,


  • Article: Braakhuis BJM, Snijders PJF, Keune W-JH, Meijer CJLM, Ruijter-Schippers HJ, Leemans CR, et al. Genetic Patterns in Head and Neck Cancers that Contain or Lack Transcriptionally Active Human Papillomavirus. J Natl Cancer Inst 2004;96:998-1006.
  • Editorial: Mao L, Hong WK. How Does Human Papillomavirus Contribute to Head and Neck Cancer Development? J Natl Cancer Inst 2004;96:978-80.

    Note: The Journal of the National Cancer Institute is published by Oxford University Press and is not affiliated with the National Cancer Institute. Attribution to the Journal of the National Cancer Institute is requested in all news coverage. Visit the Journal online at

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